Evidence map›Paper›PMID 26283199›Full record

ArticleThe Journal of general physiology2015

Constitutive and ghrelin-dependent GHSR1a activation impairs CaV2.1 and CaV2.2 currents in hypothalamic neurons.

Eduardo Javier López Soto, Francina Agosti, Agustina Cabral, Emilio Roman Mustafa, Valentina Martínez Damonte, Maria Alejandra Gandini, Silvia Rodríguez, Daniel Castrogiovanni, Ricardo Felix, Mario Perelló and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Ghrelin Modulates Voltage-Gated CaMolecular pharmacology · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. The life cycle of voltage-gated CaNeuronal signaling · 2021
    Review
  11. Article
  12. Ghrelin-Mediated Regeneration and Plasticity After Nervous System Injury.Frontiers in cell and developmental biology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Ghrelin Signaling: GOAT and GHS-R1a Take a LEAP in Complexity.Trends in endocrinology and metabolism: TEM · 2020
    Review
  18. Ghrelin Selectively Inhibits CaMolecular neurobiology · 2020
    Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Eduardo Javier López SotoLaboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina.
Francina AgostiLaboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina.
Agustina CabralLaboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina.
Emilio Roman MustafaLaboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina.
Valentina Martínez DamonteLaboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina.
Maria Alejandra GandiniDepartment of Cell Biology, Center for Research and Advanced Studies of the National Polytechnic Institute, 07000 México D.F., México.
Silvia RodríguezLaboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina.
Daniel CastrogiovanniLaboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina Laboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina.
Ricardo FelixDepartment of Cell Biology, Center for Research and Advanced Studies of the National Polytechnic Institute, 07000 México D.F., México.
Mario PerellóLaboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina.
Jesica RaingoLaboratory of Electrophysiology and Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE), B1904CMA La Plata, Buenos Aires, Argentina jraingo@imbice.gov.ar.
Instituto Multidisciplinario de Biología Celular · ARInstituto Politécnico Nacional · MX

Funding

Role of the Central Amygdala in Ghrelin-Mediated Reward-Based Eating BehaviorR03TW008925 · FIC · UT SOUTHWESTERN MEDICAL CENTER · PI ZIGMAN, JEFFREY M · 2012 to 2013
$121k
FIC NIH HHS R03 TW008925FIC NIH HHS R03TW008925-01A1
6 · The paper itself

Abstract

The growth hormone secretagogue receptor type 1a (GHSR1a) has the highest known constitutive activity of any G protein-coupled receptor (GPCR). GHSR1a mediates the action of the hormone ghrelin, and its activation increases transcriptional and electrical activity in hypothalamic neurons. Although GHSR1a is present at GABAergic presynaptic terminals, its effect on neurotransmitter release remains unclear. The activities of the voltage-gated calcium channels, CaV2.1 and CaV2.2, which mediate neurotransmitter release at presynaptic terminals, are modulated by many GPCRs. Here, we show that both constitutive and agonist-dependent GHSR1a activity elicit a strong impairment of CaV2.1 and CaV2.2 currents in rat and mouse hypothalamic neurons and in a heterologous expression system. Constitutive GHSR1a activity reduces CaV2 currents by a Gi/o-dependent mechanism that involves persistent reduction in channel density at the plasma membrane, whereas ghrelin-dependent GHSR1a inhibition is reversible and involves altered CaV2 gating via a Gq-dependent pathway. Thus, GHSR1a differentially inhibits CaV2 channels by Gi/o or Gq protein pathways depending on its mode of activation. Moreover, we present evidence suggesting that GHSR1a-mediated inhibition of CaV2 attenuates GABA release in hypothalamic neurons, a mechanism that could contribute to neuronal activation through the disinhibition of postsynaptic neurons.

Indexed as

AnimalsBase SequenceCalciumCalcium Channels, N-TypeCalcium SignalingCells, CulturedGhrelinHEK293 CellsHumansHypothalamusIon Channel GatingMiceMolecular Sequence DataNeuronsRatsRats, Sprague-DawleyCacna1b protein, ratCalciumCalcium Channels, N-TypeGhrelinGhsr1a protein, ratReceptors, Ghrelin

Identifiers

PMID26283199
PMCPMC4555474
OpenAlexW2131830608

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.